Key result
Serum periostin is ~35% higher in Crohn's disease, while its deficiency attenuates intestinal fibrosis in mice.
Why the study?
Crohn's disease is characterized by excessive intestinal fibrosis, and periostin is known to be important in fibrosis development, but its role in the pathogenesis of Crohn's disease remained to be investigated.
Does periostin play a role in the development of intestinal fibrosis in Crohn's disease?
Case-Control (n=225)
Does periostin play a role in the development of intestinal fibrosis in Crohn's disease?
Periostin is highly expressed in Crohn's disease patients and plays a crucial role in the development of intestinal fibrosis, suggesting it may serve as a biomarker or therapeutic target.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for periostin in CD fibrosis; prospective trials needed before clinical adoption as biomarker or therapeutic target.
BACKGROUND AND AIM: Crohn's disease (CD) is a chronic inflammatory bowel disease characterized by excessive intestinal fibrosis. We previously demonstrated that periostin is highly expressed in various fibrosis-related diseases and is important in the development of fibrosis. In this study, we aimed to investigate the role of periostin in the pathogenesis of CD. METHODS: We evaluated periostin expression in the terminal ileum of CD patients. We examined serum periostin levels in 75 CD patients and 150 healthy controls. We applied periostin-deficient (PNKO) and wild-type (WT) mice to a mouse model mimicking CD induced by repeated intrarectal administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS). RESULTS: Periostin was highly expressed in the stenotic areas of CD patients compared with controls, correlated with the severity of intestinal fibrosis. Serum periostin levels were significantly higher in CD patients than in healthy controls (88.5 ng/mL vs. 65.5 ng/mL; p < 0.01). In the mice with TNBS-induced colitis, periostin was highly expressed transmurally in the intestines, similar to CD patients. Fibrosis scores, collagen deposition, and phosphorylation of Smad3 were significantly increased in WT mice, whereas these were attenuated in PNKO mice. CONCLUSIONS: CD patients showed significantly high expression of periostin in both tissues and serum. Taken together with its important role in the underlying mechanism of fibrosis in the TNBS-treated mice, periostin is involved in the development of fibrosis in CD patients.
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Takedomi et al. (2026) conducted a case-control in Crohn's disease (n=225). Periostin expression vs. Healthy controls was evaluated on Serum periostin levels (ng/mL) (p=< 0.01). Serum periostin levels were significantly higher in Crohn's disease patients than healthy controls (88.5 vs 65.5 ng/mL; p<0.01), and periostin deficiency attenuated intestinal fibrosis in mice.
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